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/mammalian target of rapamycin (PI3K/mTOR) cascade is a characterized mechanism of endocrine resistance, with aberrant stimulation promoting estrogen receptor (ER) α (ESR1) activation and tumor growth, despite estrogen antagonizing- or estrogen restriction
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
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Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
Division of Environmental Genetics and Molecular Toxicology, Division of Epidemiology and Biostatistics, Center for Environmental Genetics, Cancer Center, Department of Pathology, Department of Pathology and Laboratory Medicine, Department of Environmental Health
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. 1988 ), a thesis supported by animal studies ( Prins 1997 , Ho et al . 2006 , Prins & Korach 2008 ). Estrogen receptors (ER), ERα and ERβ, are the major mediators of estrogen signaling. Upon binding of estradiol-17β, ER in the nucleus forms a homo
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) Chakraborty S Willett H Biswas PK 2012 Insight into estrogen receptor beta-beta and alpha-beta homo- and heterodimerization: a combined molecular dynamics and sequence analysis study . Biophysical Chemistry 42 – 50 . ( https://doi.org/10.1016/j
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cancers whose development and growth are initially steroid hormone-dependent ( Metcalfe et al. 2018 , Dhiman et al. 2018 ). The family of SRs consists of estrogen receptor (ER), and 3-ketosteroid receptors (NR3Cs), glucocorticoid (GR, NR3C1
Department of Cancer Cell Biology, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin, People’s Republic of China
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Department of Clinical Sciences, College of Medicine, University of South Florida, Tampa, Florida, USA
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Department of Clinical Sciences, College of Medicine, University of South Florida, Tampa, Florida, USA
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ER-negative breast cancer includes most aggressive subtypes of breast cancer such as triple negative (TN) breast cancer. Excluded from hormonal and targeted therapies effectively used for other subtypes of breast cancer, standard chemotherapy is one of the primary treatment options for these patients. However, as ER− patients have shown highly heterogeneous responses to different chemotherapies, it has been difficult to select most beneficial chemotherapy treatments for them. In this study, we have simultaneously developed single drug biomarker models for four standard chemotherapy agents: paclitaxel (T), 5-fluorouracil (F), doxorubicin (A) and cyclophosphamide (C) to predict responses and survival of ER− breast cancer patients treated with combination chemotherapies. We then flexibly combined these individual drug biomarkers for predicting patient outcomes of two independent cohorts of ER− breast cancer patients who were treated with different drug combinations of neoadjuvant chemotherapy. These individual and combined drug biomarker models significantly predicted chemotherapy response for 197 ER− patients in the Hatzis cohort (AUC = 0.637, P = 0.002) and 69 ER− patients in the Hess cohort (AUC = 0.635, P = 0.056). The prediction was also significant for the TN subgroup of both cohorts (AUC = 0.60, 0.72, P = 0.043, 0.009). In survival analysis, our predicted responder patients showed significantly improved survival with a >17 months longer median PFS than the predicted non-responder patients for both ER− and TN subgroups (log-rank test P-value = 0.018 and 0.044). This flexible prediction capability based on single drug biomarkers may allow us to even select new drug combinations most beneficial to individual patients with ER− breast cancer.
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Background In estrogen receptor (ER)-positive breast cancer, progesterone receptor (PR) expression is generally considered a marker of an intact estrogen-responsive pathway ( Horwitz & McGuire 1975 ). In addition, patients with ER
Department of Pathology, Yonsei University College of Medicine, Seoul, South Korea
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Department of Pathology, Yonsei University College of Medicine, Seoul, South Korea
Severance Biomedical Science Institute (SBSI), Yonsei University College of Medicine, Seoul, South Korea
Global 5-5-10 System Biology, Yonsei University, Seoul, South Korea
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et al . 2005 , Janni et al . 2011 ). Recurrence after long period of dormancy is especially common in estrogen receptor-positive (ER+) breast cancer ( Han et al . 2016 , Zhang et al . 2013 ). While estrogen receptor-negative (ER−) cancer rarely
Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Department of Immunology, Manitoba Institute of Cell Biology, Department of Biochemistry and Medical Genetics, University of Manitoba, 471 Apotex Centre 750 McDermot Avenue, Winnipeg, Manitoba, Canada R3E 0T5
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Introduction Estrogen signaling through estrogen receptor α (ERα) is pivotal to the survival and maintenance of ERα + breast cancer tumors. Furthermore, the estrogen–ERα signaling axis has been shown to be indispensable to mammary gland development
Section of Oncology, Department of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway
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Section of Oncology, Department of Oncology, Department of Clinical Science, University of Bergen, Bergen, Norway
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( Lønning et al . 1990 ). Thus, aromatization of androstenedione into E 1 is the major pathway of estrogen synthesis in postmenopausal women. While E 1 is inactive by itself with respect to stimulating estrogen receptor activation, it is easily converted
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are recognized as co-mediators of tumor progression rather than as merely bystanders. Estrogen is well recognized as a mitogen for breast cancer cells. Traditionally, estrogenic effects have been ascribed to the nuclear estrogen receptors (ERα and ERβ